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PY3.1-12 | Nerve and Muscle Physiology — Practice Quiz

Practice 12 questions · Untimed · Unlimited attempts

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Q1 PY3.2 1 pt

The resting membrane potential of a typical neuron is approximately -70 mV. This is closest to the equilibrium potential of which ion?

A Na+ (E_Na = +61 mV)
B K+ (E_K = -94 mV)
C Ca²+ (E_Ca = +123 mV)
D Cl- (E_Cl = -76 mV)

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Q2 PY3.3 1 pt

During the rising phase (depolarisation) of a nerve action potential, the membrane potential moves rapidly from -55 mV toward +30 mV. This is caused by:

A Opening of voltage-gated K+ channels and K+ efflux
B Activation of the Na+/K+-ATPase pump
C Opening of voltage-gated Na+ channels and Na+ influx via positive feedback
D Closure of K+ leak channels and accumulation of intracellular K+

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Q3 PY3.4 1 pt

A nerve conduction study shows a conduction velocity of 1.0 m/s. Based on the Erlanger-Gasser classification, this fibre is most likely:

A Type Aα — motor to skeletal muscle
B Type Aδ — fast pain and temperature
C Type B — preganglionic autonomic
D Type C — slow pain, postganglionic autonomic

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Q4 PY3.1 1 pt

A patient with Guillain-Barré syndrome has autoimmune destruction of Schwann cells in peripheral nerves. The primary physiological consequence is:

A Loss of neurotransmitter synthesis in the neuron cell body
B Disruption of saltatory conduction, severely reducing conduction velocity
C Destruction of nicotinic receptors at the neuromuscular junction
D Depletion of acetylcholinesterase in the synaptic cleft

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Q5 PY3.5 1 pt

At a chemical synapse, the entry of which ion into the presynaptic terminal is the essential trigger for neurotransmitter release?

A Na+
B K+
C Ca²+
D Cl-

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Q6 PY3.6 1 pt

A patient with myasthenia gravis has antibodies against nicotinic ACh receptors. After repeated nerve stimulation at 3 Hz, the compound muscle action potential (CMAP) shows a progressive decrease in amplitude (decrement). This occurs because:

A ACh release from the motor neuron decreases with each stimulus
B The reduced number of receptors causes the end-plate potential to fall below the safety factor with repeated stimulation
C The Na+/K+-ATPase cannot keep up with repeated action potentials
D Myosin ATPase activity is directly inhibited by the antibodies

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Q7 PY3.7 1 pt

In the cross-bridge cycle of skeletal muscle contraction, which step requires the binding of a new ATP molecule to the myosin head?

A Formation of the cross-bridge (myosin binding to actin)
B The power stroke (pivoting of the myosin head)
C Detachment of the myosin head from actin
D Binding of Ca²+ to troponin C

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Q8 PY3.8 1 pt

A muscle biopsy shows fibres that are rich in myoglobin, have abundant mitochondria, and are highly resistant to fatigue. These are most likely:

A Type IIb (fast glycolytic) fibres
B Type IIa (fast oxidative-glycolytic) fibres
C Type I (slow oxidative) fibres
D Cardiac muscle fibres

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Q9 PY3.9 1 pt

During fused (complete) tetanus, the muscle produces sustained maximal force because:

A Each action potential is larger in amplitude than the previous one
B Stimuli arrive faster than Ca²+ can be pumped back into the SR, maintaining high cytoplasmic Ca²+
C More motor units are recruited with each successive stimulus
D ATP production increases with each contraction cycle

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Q10 PY3.10 1 pt

A drug that inhibits myosin light chain kinase (MLCK) would most directly affect contraction in:

A Skeletal muscle, because MLCK phosphorylates troponin
B Cardiac muscle, because MLCK initiates Ca²+-induced Ca²+ release
C Smooth muscle, because MLCK phosphorylation of myosin light chains is required to activate cross-bridge cycling
D All three muscle types equally, because MLCK is the universal contraction trigger

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Q11 PY3.11 1 pt

The mechanism by which Ca²+ triggers contraction in cardiac muscle differs from skeletal muscle. In cardiac muscle, the process is called:

A Direct mechanical coupling of DHPR to RyR1
B Ca²+-induced Ca²+ release (CICR) via RyR2
C Calmodulin-dependent myosin phosphorylation
D IP3-mediated Ca²+ release from the SR

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Q12 PY3.12 1 pt

An athlete completes a 100-metre sprint in 10 seconds. During the first 8 seconds, the primary source of ATP for muscle contraction was:

A Aerobic oxidative phosphorylation of fatty acids
B Anaerobic glycolysis producing lactate
C The phosphocreatine (PCr) system via creatine kinase
D Oxidation of branched-chain amino acids

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